On Tuesday, the two feuding parties of the CRISPR gene editing patent fight entered the boxing ring: attorneys for each side made oral arguments before three-judge panel, in a case that not only puts billions of potential dollars at stake, but could define the future of genetic engineering.
In Brief
Though aging seems like one of the most natural things, an affair common to all living creatures, the process is actually poorly understood by scientists. A new study detailed in Nature aims to shed light on the phenomenon as a research team led by the Harvard T.H. Chan School of Public Health has uncovered a relationship between lifespan and RNA splicing, a core function of cells that allows a single gene to produce a variety of proteins.
The researchers already knew that mutations in RNA splicing could lead to disease, but they wanted to find out if the act of splicing itself had an impact on the aging process. To find out, they designed experimental setups using the roundworm Caenorhabditis elegans, which show visible signs of aging during their short three-week lifespan.
Great.
Research published in Acta Neuropathologica, identified alterations in a protein known as ATRX in human brain tumours; researchers might also be able to target microRNAs directly, altering their levels to make cancer cells less likely to form tumours.
A recent study suggests that two recently discovered genetic differences between brain cancer cells and normal tissue cells could offer clues to tumour behaviour and potential new targets for therapy.
Published in Acta Neuropathologica, the study identified alterations in a protein known as ATRX in human brain tumours that arise as part of a genetically inherited condition known as neurofibromatosis type 1 (NF1). The disorder, marked initially by benign tumours on nerves, often leads to brain cancer, and although most NF1-related malignancies are nonaggressive, a fraction are “high-grade” and difficult to treat, experts say.
More on the cell circuited technology that will deprive cancer cells of oxygen.
Imagine having cells in your body that can actively repel cancer in a way that makes it theoretically impossible for you to suffer from it.
Researchers at the U.K.’s University of Southampton…have engineered cells with a so-called “built-in genetic circuit” capable of producing a molecule for inhibiting the ability of tumors to grow and survive in the body.
“There are various defense mechanisms built into human cells, such as proteins that spot DNA damage, but there are also gaps in this defense system that are exploited by disease,” Professor Ali Tavassoli, one of the lead authors of the paper …“We were wondering if it is possible to equip human cells with the ability to sense and respond to a disease marker…”
The CLONED dogs of war: Russia unveils genetically-enhanced canines which will work with Putin’s Special Forces and were created by scientist attempting to restore woolly mammoths
A look back at one of the milestones for SRF and the first successful fundraiser on Lifespan.io for MitoSENS.
We need your support at this critical juncture of the MitoSENS project. The MitoSENS team has already demonstrated the rescue of cells containing mitochondrial mutations, and has recently generated highly promising preliminary data showing the rescue of the complete loss of a mitochondrial gene. Our next steps will focus on improving the effectiveness of the targeting system, so that we can repeat our success with one mitochondrial gene to all thirteen. We will then transition this work into animal models of mitochondrial dysfunction. This would be a crucial step in what may be the development of an eventual cure for aging and aging related diseases.
We have a talented team of highly trained mitochondrial biologists working on MitoSENS. Right now the rate-limiting factor is the cost of the expensive reagents that we use for these experiments. Increasing our funding with this campaign will allow us to double the pace of our research and bring results to the public that much faster. We have made preliminary progress on rescuing function with a second gene, ATP6, and your support will help us perfect our targeting of both ATP8 and ATP6. This requires more cells, more viruses, and many new synthetic gene sequences. Specifically, we will spend your generous donations on cell culture reagents, oxygen consumption measurements, virus production, quantitative reverse transcription PCR, DNA synthesis services, and publication of our results in a peer-reviewed journal.
Your support will help take us there.